SS-31
Elamipretide / MTP-131 / Bendavia
Mitochondria-targeted tetrapeptide that protects the inner mitochondrial membrane. Reduces oxidative stress and restores ATP production. In Phase II and III clinical trials for heart failure and Barth syndrome.
Mechanism of action
Targets cardiolipin on mitochondrial inner membrane — the site of ATP production. Prevents electron leak reduces reactive oxygen species production and maintains mitochondrial membrane potential. Restores ATP production in damaged or aging mitochondria through direct membrane stabilization.
Effects in the body
SS-31 goes directly to the mitochondria and protects the inner membrane where ATP is produced. In aging and disease this membrane gets progressively damaged. SS-31 specifically stabilizes cardiolipin to restore efficient energy production across multiple tissue types.
Pros & cons (from the literature)
- In Phase II and III clinical trials — most advanced mitochondrial peptide
- Targeted mitochondrial protection with clear mechanism
- Multiple disease application potential
- Strong preclinical data for heart kidney and muscle
- Unique cardiolipin targeting mechanism
- Currently RUO not compoundable in USA
- Injectable only no oral form
- Clinical trials have shown mixed results so far
- Very expensive in clinical trial formulation
- Not yet approved for any indication
Protocol summary (from published research)
Dosing ranges reproduced from published research literature. Not a prescription, not medical advice.
FDA & regulatory status
Evidence base
Phase II and III trial data exists. Szeto et al. foundational papers well cited. Barth syndrome Phase III data most advanced. Mixed efficacy results in heart failure trials.
Primary research sources
Peer-reviewed literature referenced throughout this profile is drawn from PubMed, Cell Metabolism, and clinical trial registries cited in the evidence base above.